Protection from experimental ventilator-induced acute lung injury by IL-1 receptor blockade

Frank, James A.; Pittet, Jean–François; Wray, Charlie M; Matthay, Michael A.

doi:10.1136/thx.2007.079608

Cited by 104 publications

(109 citation statements)

References 46 publications

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“…Many studies have shown that severe lung injury is provoked by ventilation with high tidal volumes. [15][16][17] Although the exact underlying mechanisms of VILI remain undefined, several potential pathways have been proposed, with barotrauma appearing to be the generally accepted one. In our study, significant infiltration of neutrophils was observed on pathological examination of the lung tissue exposed to high tidal volume ventilation.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane attenuates pulmonary inflammation and ventilator-induced lung injury by upregulation of HO-1 mRNA expression in mice

Xiong¹,

Lin²,

Wang³

2013

IJN

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Background: Mechanical ventilation has been documented to paradoxically cause lung injury. As a commonly used volatile anesthetic, sevoflurane has been proven to possess antiinflammatory and antioxidative properties. This study aims to investigate the protective effects of sevoflurane on inflammation and ventilator-induced lung injury during mechanical ventilation in healthy mice. Methods: The adult healthy mice were divided into four groups, each consisting of ten subjects: mice in group Con-L VT and group Sev-L VT were ventilated with tidal volumes of 8 mL/kg for 4 hours, while those in group Con-H VT and group Sev-H VT were ventilated with tidal volumes of 16 mL/kg instead. Control mice (group Con-L VT and Con-H VT ) were subjected to fresh air, while sevoflurane-treated mice (groups Sev-L VT and Sev-H VT ) were subjected to air mixed with 1 vol% sevoflurane. After 4 hours of ventilation, the bronchoalveolar lavage (BAL) fluid was collected and analyzed for the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10. Lung homogenates were harvested to detect the expression of nuclear factorkappa B (NF-κB) and heme oxygenase (HO)-1 mRNA by reverse transcription-polymerase chain reaction method. Lung damage was evaluated using the modified Ventilator-Induced Lung Injury histological scoring system. Results: Compared to group Con-L VT , the levels of TNF-α, IL-1β, IL-6, and IL-10 in BAL fluid, mRNA expressions of NF-κB and HO-1 in lung tissue, and lung injury scores were significantly increased in group Con-H VT ; compared to group Con-H VT , group Sev-H VT BAL samples showed decreased levels of TNF-α, IL-1β, and IL-6; they also showed increased levels of IL-10, the downregulation of NF-κB mRNA, and HO-1 mRNA upregulation; the lung injury scores were significantly lower in group Sev-H VT than group Con-H VT . Conclusion: Mechanical ventilation with high tidal volume might lead to lung injury, which could be significantly, but not completely, attenuated by sevoflurane inhalation by inhibiting the NF-κB-mediated proinflammatory cytokine generation and upregulating HO-1 expression.

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Section: Discussionmentioning

confidence: 99%

Sevoflurane attenuates pulmonary inflammation and ventilator-induced lung injury by upregulation of HO-1 mRNA expression in mice

Xiong¹,

Lin²,

Wang³

2013

IJN

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“…IL-1β expression augments neutrophil recruitment and also impairs fluid clearance via down-regulation of the epithelial sodium channel (ENaC) [94]. Early blockage of IL-1β is protective in a murine model of VILI, suggesting that IL-1β may be a potential target in ALI [92]. However, IL-1β has some roles in epithelial wound repair [95,96], and further evaluation of its role in both the pathogenesis and resolution of ALI is needed.…”

Section: Release Of Other Proinflammatory Mediatorsmentioning

confidence: 99%

“…Other inflammatory mediators, such as IL-1β, have been found to be upregulated in animal models of ALI as well as in BAL fluid from patients with ARDS [92,93]. IL-1β expression augments neutrophil recruitment and also impairs fluid clearance via down-regulation of the epithelial sodium channel (ENaC) [94].…”

Section: Release Of Other Proinflammatory Mediatorsmentioning

confidence: 99%

“…Thus, further studies are needed to better define the interplay of H 2 S and substance P in mediating ALI. Although animal studies suggest modification of these pathways may be a novel target to mitigate lung injury, additional studies are warranted.Other inflammatory mediators, such as IL-1β, have been found to be upregulated in animal models of ALI as well as in BAL fluid from patients with ARDS [92,93]. IL-1β expression augments neutrophil recruitment and also impairs fluid clearance via down-regulation of the epithelial sodium channel (ENaC) [94].…”

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confidence: 99%

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Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

118

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Acute lung injury (ALI) is a clinical disease marked by respiratory failure due to disruption of the epithelial and endothelial barrier, flooding of the alveolar compartment with protein-rich fluid and recruitment of neutrophils into the alveolar space. ALI affects approximately 200,000 patients annually in the USA and results in approximately 75,000 deaths. It is associated with prolonged mechanical ventilation, intensive medical care, high morbidity and mortality, and rising healthcare costs. Owing to its impact on public health, great strides have been made towards understanding the pathobiology of ALI to affect outcome. This review will focus on the role of the epithelial cell in the pathogenesis and resolution of ALI and the role of various inflammatory mediators in ALI. Keywordsβ2-agonist; acute lung injury; acute respiratory distress syndrome; chemokine; cytokine; epithelial cell; inflammation; methylprednisolone; neutrophil; salbutamol; steroid; ventilator-induced lung injuryAcute lung injury/acute respiratory distress syndrome (ALI/ARDS) was first described in 1967 by Ashbaugh and colleagues in a group of 12 patients who shared a constellation of clinical symptoms including acute respiratory distress, hypoxemia refractory to supplemental oxygen, decreased lung compliance and diffuse pulmonary infiltrates [1]. Since this first description, the clinical criteria have evolved to include acute onset of respiratory distress, bilateral pulmonary infiltrates seen on chest radiographs, absence of left-sided heart failure and hypoxemia, with the severity of hypoxemia distinguishing ALI and ARDS (Box 1) [2]. Extrapolating from recent epidemiologic studies using these criteria, ALI affects about 200,000 patients annually in the USA and results in approximately 75,000 deaths [3]. This disease, which can be caused by common events such as pneumonia, sepsis and trauma, results in high morbidity, mortality and healthcare expenditures associated with prolonged mechanical ventilation and intensive care. Because of its impact on public health and patient outcomes, great strides have been made towards understanding the pathobiology of ALI.When defined broadly to include all processes related to defense against microbes, other environmental insults and injury, a wide variety of cell types and proteins participate in inflammation and immunity. Leukocytes are the paradigmatic inflammatory cell type, but they are not the only cells that function in defense and immunity. The epithelial lining of all tissues forms a continuous barrier to the environment and is the first line of defense against infectious agents and toxins. Though specialized to serve distinct functions among tissues, epithelial cells respond similarly to injury and infection, and regulate leukocyte influx through the production of proinflammatory cytokines, chemokines and other factors that modulate chemokine gradients and effect leukocyte migration. This review will focus on the role of the pulmonary epithelium and inflammatory mediators in ALI. More s...

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“…KC and MCP-1 are chemotactic signals for neutrophils, which contribute to the development of VILI [17,18]. IL-1β was shown to induce endothelial permeability and aggravate VILI [19]. IL-6 is upregulated under mechanical ventilation and, although its exact role in VILI remains controversial, IL-6 levels are correlated with organ failure and outcome in ARDS [20][21][22][23].…”

Section: Discussionmentioning

confidence: 99%

Increasing the inspiratory time and I:E ratio during mechanical ventilation aggravates Ventilator-induced lung injury in mice

Müller-Redetzky¹,

Felten²,

Polikarpova³

et al. 2014

Pneumologie

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Introduction: Lung-protective ventilation reduced acute respiratory distress syndrome (ARDS) mortality. To minimize ventilator-induced lung injury (VILI), tidal volume is limited, high plateau pressures are avoided, and positive end-expiratory pressure (PEEP) is applied. However, the impact of specific ventilatory patterns on VILI is not well defined. Increasing inspiratory time and thereby the inspiratory/expiratory ratio (I:E ratio) may improve oxygenation, but may also be harmful as the absolute stress and strain over time increase. We thus hypothesized that increasing inspiratory time and I:E ratio aggravates VILI. Methods: VILI was induced in mice by high tidal-volume ventilation (HV T 34 ml/kg). Low tidal-volume ventilation (LV T 9 ml/kg) was used in control groups. PEEP was set to 2 cm H 2 O, FiO 2 was 0.5 in all groups. HV T and LV T mice were ventilated with either I:E of 1:2 (LV T 1:2, HV T 1:2) or 1:1 (LV T 1:1, HV T 1:1) for 4 hours or until an alternative end point, defined as mean arterial blood pressure below 40 mm Hg. Dynamic hyperinflation due to the increased I:E ratio was excluded in a separate group of animals. Survival, lung compliance, oxygenation, pulmonary permeability, markers of pulmonary and systemic inflammation (leukocyte differentiation in lung and blood, analyses of pulmonary interleukin-6, interleukin-1β, keratinocyte-derived chemokine, monocyte chemoattractant protein-1), and histopathologic pulmonary changes were analyzed. Results: LV T 1:2 or LV T 1:1 did not result in VILI, and all individuals survived the ventilation period. HV T 1:2 decreased lung compliance, increased pulmonary neutrophils and cytokine expression, and evoked marked histologic signs of lung injury. All animals survived. HV T 1:1 caused further significant worsening of oxygenation, compliance and increased pulmonary proinflammatory cytokine expression, and pulmonary and blood neutrophils. In the HV T 1:1 group, significant mortality during mechanical ventilation was observed.

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Protection from experimental ventilator-induced acute lung injury by IL-1 receptor blockade

Cited by 104 publications

References 46 publications

Sevoflurane attenuates pulmonary inflammation and ventilator-induced lung injury by upregulation of HO-1 mRNA expression in mice

Sevoflurane attenuates pulmonary inflammation and ventilator-induced lung injury by upregulation of HO-1 mRNA expression in mice

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Increasing the inspiratory time and I:E ratio during mechanical ventilation aggravates Ventilator-induced lung injury in mice

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